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Relationship between vasoactive intestinal peptide and intrapulmonary vascular dilatation in children with various
V Chongsrisawat1, S Ampai, P Chotivitayatarakorn
1Department of Paediatrics, Faculty of Medicine, Chulalongkorn University & Hospital, Bangkok, Thailand.
Insights
Vasoactive intestinal peptide (VIP) is not solely responsible for intrapulmonary vascular dilatation (IVD) in hepatopulmonary syndrome (HPS). Contrast-enhanced echocardiography (CEE) effectively detects IVD early in children with liver disease.
Area of Science:
- Pediatric Gastroenterology
- Pulmonology
- Hepatology
Background:
- Hepatopulmonary syndrome (HPS) involves liver dysfunction, intrapulmonary vascular dilatation (IVD), and hypoxemia.
- The exact pathogenesis of HPS remains unclear, but vasodilators like vasoactive intestinal peptide (VIP) are suspected contributors to pulmonary vascular abnormalities.
- Contrast-enhanced echocardiography (CEE) can identify IVD before significant gas exchange impairment.
Purpose of the Study:
- To investigate the role of vasoactive intestinal peptide (VIP) in the development of intrapulmonary vascular dilatation (IVD) within hepatopulmonary syndrome (HPS).
- To assess the utility of contrast-enhanced echocardiography (CEE) for early IVD detection in pediatric liver disease patients.
Main Methods:
- Forty-two children with liver disease underwent testing for oxygen saturation, CEE (agitated saline technique), liver function, and serum VIP levels.
- Patients were recruited from a pediatric liver clinic over a one-year period.
- Serum VIP levels were compared between children with liver disease and controls, and between CEE-positive and CEE-negative groups.
Main Results:
- 33% of the pediatric patients with liver disease showed positive CEE results, indicating IVD.
- Serum VIP levels were significantly higher in children with liver disease compared to controls (p=0.03).
- CEE-positive children had a trend towards higher serum VIP levels, though not statistically significant (p=0.3).
Conclusions:
- Contrast-enhanced echocardiography (CEE) serves as a valuable non-invasive tool for the early detection of IVD in pediatric liver disease.
- Vasoactive intestinal peptide (VIP) alone does not appear to be the sole cause of IVD in HPS.
- Further research is needed to identify the specific causative agents of IVD in HPS.
Aim:
To evaluate the potential of vasoactive intestinal peptide (VIP) as a pathogenic factor of intrapulmonary vascular dilatation (IVD) in hepatopulmonary syndrome (HPS).
Background:
HPS comprises a triad comprising liver dysfunction, IVD and hypoxaemia. Although the pathogenesis of the process has not been elucidated, many vasodilating substances, such as VIP, have been implicated in the development of pulmonary vascular abnormalities. IVD can be detected by contrast-enhanced echocardiography (CEE) before the development of abnormal gas exchange.
Methods:
Forty-two children (20M, 22F; mean age 4.39 +/- 4.17 y) with various liver diseases who attended the paediatric liver clinic of King Chulalongkorn Memorial Hospital between March 2000 and February 2001 were recruited to the study. Each patient was tested for transcutaneous O2 saturation, CEE (applying the agitated normal saline technique), liver function test and serum VIP level.
Results:
Fourteen of the 42 patients (33%) were CEE positive. Only one of the 14 patients had associated hypoxia and clinical cyanosis. The serum VIP levels of children with liver disease were significantly higher than those of the controls (60.21 +/- 35.04 pg/ml vs 43.71 +/- 34.61 pg/ml, p = 0.03). CEE-positive children tended to have higher serum VIP levels than CEE-negative children (72.65 +/- 40.31 vs 53.99 +/- 31 pg/ml, p = 0.3). The serum VIP levels of biliary atresia (BA) patients with favourable outcomes (serum bilirubin < or = 34 micromol/L) were not significantly different from those with unfavourable outcomes (serum bilirubin > 34 micromol/L) (42.95 +/- 14.53 pg/ml vs 66.07 +/- 32.17 pg/ml, p = 0.5).
Conclusions:
CEE is a non-invasive test for early detection of IVD in children with liver disease. VIP is not solely responsible for the pathogenesis of IVD in HPS. Further studies are required to determine which substances cause the development of IVD.
